Microarray analysis of the Ler regulon in enteropathogenic and enterohaemorrhagic Escherichia coli strains.
Microarray analysis of the Ler regulon in enteropathogenic and enterohaemorrhagic Escherichia coli strains.
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DOI：
10.1371/journal.pone.0080160
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Pallen MJ
中科院分区：
文献类型：
--
作者：
Bingle LE;Constantinidou C;Shaw RK;Islam MS;Patel M;Snyder LA;Lee DJ;Penn CW;Busby SJ;Pallen MJ
III型蛋白分泌系统是肠致病性和肠出血性大肠杆菌致病型的重要致病因子。编码该装置的基因位于致病岛（肠上皮细胞消失的位点）上，并由主调节因子Ler转录激活。在每种致病型中，Ler也被认为调节位于染色体其他位置的基因，但Ler调节子的完整范围尚不清楚，特别是对于肠致病性大肠杆菌。杆菌对两株大肠杆菌的Ler调节子进行了定义。大肠杆菌：E2348/69（肠致病性）和EDL 933（肠出血性）在中期和晚期对数生长期通过DNA微阵列分析的转录组的野生型和每个菌株的ler突变版本。在这两种菌株中，Ler调节子集中在肠上皮细胞消失的位点上-所有主要的转录单位都被Ler激活，唯一的例外是E2348/69中对数中期生长期间的LEE 1操纵子。然而，Ler调节子确实延伸得更广，并且还包括未连锁的致病性基因：在E2348/69中，该基因座外的50多个基因受到调节，包括许多已知或潜在的致病性决定子;在EDL 933中，仅4个额外的LEE基因被激活，再次包括已知的致病性因子。在E2348/69中，其中Ler调节子明显是生长期依赖性的，发现包括质粒编码的调节操纵子perABC在内的许多基因受到Ler的负调控。PerC的Ler的负调节，其本身是ler启动子的正调节子，表明涉及这些蛋白质的负反馈环。
The type III protein secretion system is an important pathogenicity factor of enteropathogenic and enterohaemorrhagic Escherichia coli pathotypes. The genes encoding this apparatus are located on a pathogenicity island (the locus of enterocyte effacement) and are transcriptionally activated by the master regulator Ler. In each pathotype Ler is also known to regulate genes located elsewhere on the chromosome, but the full extent of the Ler regulon is unclear, especially for enteropathogenic E. coli. The Ler regulon was defined for two strains of E. coli: E2348/69 (enteropathogenic) and EDL933 (enterohaemorrhagic) in mid and late log phases of growth by DNA microarray analysis of the transcriptomes of wild-type and ler mutant versions of each strain. In both strains the Ler regulon is focused on the locus of enterocyte effacement – all major transcriptional units of which are activated by Ler, with the sole exception of the LEE1 operon during mid-log phase growth in E2348/69. However, the Ler regulon does extend more widely and also includes unlinked pathogenicity genes: in E2348/69 more than 50 genes outside of this locus were regulated, including a number of known or potential pathogenicity determinants; in EDL933 only 4 extra-LEE genes, again including known pathogenicity factors, were activated. In E2348/69, where the Ler regulon is clearly growth phase dependent, a number of genes including the plasmid-encoded regulator operon perABC, were found to be negatively regulated by Ler. Negative regulation by Ler of PerC, itself a positive regulator of the ler promoter, suggests a negative feedback loop involving these proteins.
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影响因子：
6.7
作者：
Cordeiro TN;Schmidt H;Madrid C;Juárez A;Bernadó P;Griesinger C;García J;Pons M
通讯作者：
Pons M
影响因子：
3.5
作者：
CHEREPANOV, PP;WACKERNAGEL, W
通讯作者：
WACKERNAGEL, W
影响因子：
3.2
作者：
Berdichevsky, T;Friedberg, D;Rosenshine, I
通讯作者：
Rosenshine, I
影响因子：
3.2
作者：
Iguchi, Atsushi;Thomson, Nicholas R.;Frankel, Gad
通讯作者：
Frankel, Gad
影响因子：
2.8
作者：
Abu-Ali, Galeb S.;Ouellette, Lindsey M.;Manning, Shannon D.
通讯作者：
Manning, Shannon D.